Acute hyperglycemia is related to gastrointestinal symptoms in motion sickness: an experimental study.

Motion sickness is caused by exposure to unfamiliar motions and typical symptoms of motion sickness include nausea and vomiting. To observe the metabolic and hormonal differences between nausea/vomiting (NAV) subjects and non-nausea/vomiting (NNV) ones, and to understand how the differences in metabolites and hormones affect the tolerance of organism to acceleration, 60 volunteers were exposed to repetitive acceleration using a 6-degree-of-freedom ship motion simulator. Meanwhile, 36 rats were randomly divided into three groups: an acceleration model group (n=14, exposed to acceleration), insulin group (n=14, intraperitoneal injection of insulin 30 min before exposure to acceleration), and control group (n=8). Gas chromatography coupled to time-of-flight mass spectrometry (GC-TOF/MS) was applied to analyze the serum metabolites in human subjects. Serum glucocorticoid, insulin, and glucagon levels were determined by radioimmunoassay in the NAV and NNV subjects as well as in rats, and serum epinephrine level was determined by ELISA. After acceleration exposure, 9 metabolites, including L-histidine, L-ornithine, L-serine, L-tyrosine, pyroglutamic acid, fumaric acid, urea, n-dodecanoic acid and n-tetradecanoic acid, had different changes in the NAV and NNV groups. The serum levels of 4-hydroxy-L-proline, glucose, oleic acid and urea were significantly higher in the NAV group than in the NNV group after exposure; however, only the elevation degree of serum glucose was significantly greater in the NAV group than in the NNV group (P<0.05). Serum cortisol and epinephrine were increased in both groups. Before exposure, insulin level in the NAV group was significantly lower than that in the NNV group (P<0.05). After rotation exposure, rat serum glucose in the insulin group was significantly lower than that in the acceleration model group (P<0.001), and the motion sickness index was significantly lower than that in the acceleration model group (P<0.05). Our study provides the first evidence that stable glucose level can help to relieve gastrointestinal symptoms in motion sickness, and suggests that acute hyperglycemia is related to gastrointestinal symptoms in motion sickness.

[Effects of ginsenosides extracted from ginseng stem and leaves on glucocorticoid receptor in different viscera in heat-damaged rats].

OBJECTIVE: To evaluate the effects of ginsenosides (GSS) extracted from ginseng stem and leaves on glucocorticoid receptor (GR) in different viscera in heat-damaged rats, and to find out its action mechanism. METHODS: Thirty-two male SD rats were divided into control group and experimental group, and fed 2 mg/d GSS and equal-quantity of distilled water respectively for 7 days. Eight rats of each group were exposed to (42+/-1) degrees C for one hour. The binding activities of GR in brain, thymus, lung and liver cytosols in rats were detected by radioligand binding assay. The expression levels of GR mRNA in brain and liver cytosols were determined by reverse transcription-polymerase chain reaction (RT-PCR) assay. Plasma adrenocorticotropin (ACTH) and corticosterone (CS) concentrations were determined by radioimmunoassay. RESULTS: The binding activities of GR in brain, lung and liver cytosols, and the expression levels of GR mRNA in brain and liver cytosols were all higher in the GSS-treated and heat-damaged rats than those in the untreated heat-damaged rats (P<0.05 or P<0.01). There were no significant differences in plasma concentrations of ACTH and CS between the GSS-treated heat-damaged rats and the untreated heat-damaged rats. CONCLUSION: GSS can lessen the descending degree of the binding activity of GR in brain, thymus, lung and liver cytosols, and such efficacy of GSS may be related to improvement of the expression of GR mRNA.